Which condition causes hyperphosphatemia via increased calcium citrate complexation?

Which condition causes hyperphosphatemia via increased calcium citrate complexation?

• A. Massive transfusion of citrated blood
• B. Renal failure
• C. Chemotherapy
• D. Rhabdomyolysis

Answer: (A)

Massive transfusion of citrated blood introduces a large amount of citrate into the circulation. Citrate acts as an anticoagulant by binding calcium to form calcium–citrate complexes, which readily reduces ionized calcium levels in the blood. Stored blood products also carry substantial phosphate. When large volumes are transfused, the phosphate load can raise serum phosphate, especially if clearance is overwhelmed or impaired. In this context, the combination of a large citrate (calcium-chelating) load and the phosphate from the transfused blood makes hyperphosphatemia more likely via the calcium citrate complexation pathway. Other scenarios cause hyperphosphatemia through different mechanisms: renal failure reduces excretion, tumor lysis or rhabdomyolysis release phosphate from cells, and chemotherapy can cause rapid cell turnover, but none hinge on calcium citrate complexing as the primary driver.

Massive transfusion of citrated blood introduces a large amount of citrate into the circulation. Citrate acts as an anticoagulant by binding calcium to form calcium–citrate complexes, which readily reduces ionized calcium levels in the blood. Stored blood products also carry substantial phosphate. When large volumes are transfused, the phosphate load can raise serum phosphate, especially if clearance is overwhelmed or impaired. In this context, the combination of a large citrate (calcium-chelating) load and the phosphate from the transfused blood makes hyperphosphatemia more likely via the calcium citrate complexation pathway. Other scenarios cause hyperphosphatemia through different mechanisms: renal failure reduces excretion, tumor lysis or rhabdomyolysis release phosphate from cells, and chemotherapy can cause rapid cell turnover, but none hinge on calcium citrate complexing as the primary driver.